In the PNAS Early Edition this week, researchers at Johns Hopkins University and the National Cancer Institute report the role of Hfq, an RNA chaperone in E. coli. Their study illustrates that "binding of Hfq to the rpoS mRNA is critical for [small regulatory RNA] regulation under normal conditions, but if the stability of the sRNA-mRNA complex is sufficiently high, the requirement for Hfq can be bypassed," the authors write, adding that sRNA-mRNA complex stability best predicts in vivo sRNA activity.
A trio of researchers from the Comparative Cancer Center at the University of California, Davis, shows that RNPC1, "a RNA-binding protein and a target of the p53 family, regulates p63 mRNA stability and consequently p63 activity," in PNAS this week. As overexpression of RNPC1 decreases, p63 expression is altered. "Furthermore, we showed that RNPC1 promotes keratinocyte differentiation by repressing p63 expression," the team writes, adding that their study reports a previously unknown "mechanism by which p63 expression is regulated via mRNA stability and a novel regulatory feedback loop between RNPC1 and p63."
In another PNAS Early Edition paper, researchers in the US and Germany report their deduction of "widespread genomic divergence during sympatric speciation." To test the hypothesis that the "few genes under or physically linked to loci experiencing strong disruptive selection can diverge, whereas gene flow will homogenize the remainder of the genome, resulting in isolated 'genomic islands of speciation,'" the team used a Rhagoletis pomonella model. They found widespread divergence within the Rhagoletis genome, and report that their results "highlight how the individual genes driving speciation can be embedded within an actively diverging genome."
Investigators in California and Iowa report their elucidation that a H3K36me2 histone demethylase — KDM8, formerly called JMJD5 — "acts in the cyclin A1 coding region to regulate cancer cell proliferation." In using ChIP assays and microarray experiments, the team found that "KDM8 occupies the coding region of cyclin A1 and directly regulates transcription." Further analyses showed that KDM8 is overexpressed in some cancers, the authors write.